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COMMENTARY

I Was Afraid To Check My Lp(a) but Now Know Better

Keerthana R. Pakanati, MD

DISCLOSURES November 17, 2025

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As I sat with my 30-year-old patient explaining that a lipoprotein(a) [Lp(a)] test could help us better understand their risk for coronary disease, especially since they had lost a parent to a sudden cardiac event, I hoped they would not ask: Have you checked yours? 

Because at that time, the answer was no. I was too nervous to get tested; I was unsure what I would do if it came back high. 

As a South Asian woman training to become a cardiologist, I had heard many stories of seemingly healthy “aunties and uncles” who had a massive heart attack or required multi-vessel bypass before they even retired. Yet despite my personal interest in prevention, my lack of understanding of Lp(a) held me back from getting tested. 

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Lp(a) on the Periphery

Part of the challenge is that Lp(a) long sat on the periphery of cardiovascular prevention. Although elevated levels are found in about 1 in 5 adults globally and are associated with a two- to threefold increased risk for myocardial infarction and calcific aortic valve stenosis, the test remains absent from routine clinical evaluation. This disconnect endures despite multiple societies recommending at least one lifetime measurement. While the science advanced, clinical practice lagged behind. Many clinicians hesitate to order the test (as I once did) because we were never taught what to do with the results. 

Lp(a) levels are primarily determined by genetics, although we now know that they can change throughout our lifespan. Research shows that an elevated Lp(a) level is an independent risk factor for the development of atherosclerotic, cardiovascular disease (ASCVD), and calcific aortic valve stenosis. 

It is pro-atherogenic, prothrombotic, and pro-inflammatory. For those with elevated levels, specifically in the top 5% of Lp(a) concentrations (> 90 mg/dL [190 nmol/L]), the relative risk for myocardial infarction and aortic valve stenosis is approximately two to three times higher compared to those with low levels (< 30 mg/dL [< 75 mmol/L]). 

The American Society for Preventive Cardiology (ASPC) supports measuring Lp(a) at least once in every adult to refine ASCVD risk prediction and guide more aggressive prevention strategies. The American College of Cardiology (ACC)/American Heart Association (AHA) cholesterol management guidelines recommend measuring it in individuals with a family history of premature ASCVD, unexplained ASCVD, or recurrent events despite optimal therapy. 

Given all this information, why are we not checking Lp(a) in everyone and why is it not standard of care? 

I now believe it should be. 

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The ‘Nothing Can Be Done’ Myth

The counterargument people make, and perhaps the reason I waited so long to get tested, is the inaccurate assumption that we can’t do anything about high Lp(a) levels. 

Admittedly, the most effective therapy currently available, lipoprotein apheresis, is expensive and is reserved for people with progressive coronary disease and a really high Lp(a) level despite maximum medical therapy. 

And yes, lifestyle changes, at least to our understanding, do not affect Lp(a). But we can and should focus on aggressive control of other risk factors. That means quitting smoking, getting blood pressure and A1c under control, losing weight if necessary, and eating a heart-healthy diet with a focus on whole food, plant based, or Mediterranean diets. 

And let’s not forget about lowering our low-density lipoprotein cholesterol (LDL-C). This one is paramount! A high-intensity statin should be used to reduce LDL-C as much as possible, or at least to the ACC/AHA recommendation of = 50%, with a target level of < 70 mg/dL. Keep in mind that the European guidelines recommend a goal of < 55 mg/dL. 

Although there is not yet an FDA-approved drug that directly lowers Lp(a), many therapies are on the horizon. These include antisense oligonucleotides such as pelacarsen in phase 3 clinical trials, and small interfering RNAs such as olpasiran and lepodisiran, which were shown to reduce Lp(a) by 80%-95% in early phase trials. 

It is inaccurate to say that “ nothing can be done.” We should view high Lp(a) as a marker of inherited risk that calls for earlier and more comprehensive prevention strategies. It should not be met with therapeutic inertia; it should motivate earlier and more decisive action. 

This brings me back to my patient, and to my own personal story. 

After equipping myself with the knowledge to interpret my test results, I headed to the testing booth at the ASPC conference. I now have a better understanding of just how vulnerable our patients may feel when we order lab tests, because I felt the same way. 

Now if a patient asks me, “Have you had yours checked?” I can say, “Yes, I know my Lp(a) level, and here is why I think you should check yours.” 

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Keerthana R. Pakanati, MD, is the Chief Cardiovascular Fellow at Virginia Mason Franciscan Health and host of The Heart of Prevention podcast with the American Society for Preventive Cardiology. She is passionate about preventing cardiovascular disease, caring for and educating women about their cardiovascular risk, addressing cardiovascular disparities in South Asian populations, and using media to combat medical misinformation.

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Cite this: I Was Afraid To Check My Lp(a) but Now Know Better - Medscape - November 17, 2025.